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The Journal of Nutrition Vol. 127 No. 5 May 1997, pp. 903S-906S
Copyright ©1997 by the American Society for Nutritional Sciences

Role of Kupffer Cells, Endotoxin and Free Radicals in Hepatotoxicity Due to Prolonged Alcohol Consumption: Studies in Female and Male Rats

Ronald G. Thurman, Blair U. Bradford, Yuji Iimuro, Kathryn T. Knecht, Henry D. Connor, Yukito Adachi, Chantal Wall, Gavin E. Arteel, James A. Raleigh*, Donald T. Formandagger , and Ronald P. MasonDagger

Laboratory of Hepatobiology and Toxicology, Department of Pharmacology; * Department of Radiation Oncology; and dagger  Department of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC; and Dagger  Laboratory of Molecular Biophysics, National Institute of Environmental Health Sciences, National Institute of Health, Research Triangle Park, NC

Alcohol ingestion results in increases in the release of endotoxin from gut bacteria or membrane permeability of the gut to endotoxin, or both. Female rats are more sensitive to these changes. Elevated levels of endotoxin activate Kupffer cells to release substances such as eicosanoids, tumor necrosis factor-alpha and free radicals. Prostaglandins increase oxygen uptake and most likely are responsible for the hypermetabolic state in the liver. The increase in oxygen demand leads to hypoxia in the liver, and on reperfusion, alpha -hydroxyethyl free radicals are formed that lead to tissue damage in oxygen-poor pericentral regions of the liver lobule.

Key words: alcohol-induced liver injury, endotoxin, free radicals, sex differences, rats.






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